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Biomedical subjects

G Zhao

Publications and source records attributed to G Zhao.

At least 199 records · Page 11Linked to original sources
PubMed1998

Synthesis and biological activity of binuclear platinum complexes containing two monofunctional cis-[Pt(NH3)2Cl]+ units bridged by 4,4'-dipyridyl selenides or sulfides.

The synthesis of four binuclear platinum complexes of general formula ¿cis-[Pt(NH3)2Cl]2(L)¿ (NO3)2 [L is 4,4'-dipyridyl sulfide (compound I), 4,4'-dipyridyl selenide (compound II), bis(3-methyl-4-pyridyl) sulfide (compound III) or bis(3-methyl-4-pyridyl) selenide (compound IV)] has been achieved. These compounds have been characterized by elemental analysis, IR, 1H-NMR, 13C-NMR and 195Pt-NMR spectroscopy. The above dinuclear platinum complexes have been assayed for antitumor activity in vitro against the cisplatin-sensitive L1210 (the mice leukemia) and cisplatin-insensitive HCT8 (the human coloadenocarcinoma) cell lines. The compounds show IC50 values comparable to or higher than cisplatin against L1210 cell line; however, they have lower IC50 values than cisplatin against the cisplatin-insensitive HCT8 cell line. The complexes containing S exhibit a cytotoxicity against the two cancer cell lines superior to the Se analogues. DNA binding studies indicate the compound I possibly interacts with DNA nonintercalatively. The mode of DNA binding of the dinuclear Pt(II) complexes bridged by 4,4'-dipyridyl selenides or sulfides may be different to that of the aliphatic diaminebridged dinuclear Pt(II) complexes reported previously.

Animals↗
PubMed1997

Laser Frequency-Modulated Spectroscopy of a Laser-Guided Plasma in Sodium Vapor: Line Positions for NaH (A1Sigma+-X1Sigma+), Na (9-13d and 11-14s), and Ar (5p-4s)

Laser frequency-modulated (FM) spectroscopy has been used as an axial probe of a laser-guided electric discharge in sodium-argon vapor contained in an optically accessible metal heat pipe oven. Absorption measurements in the region 23 106-23 881 cm-1 provided accurate line positions (&plusmn;<0.006 cm-1) for 141 transitions in the v' = 3-8 <-- v" = 0 and v' = 5-9 <-- v" = 1 bands of NaH (A1Sigma+-X1Sigma+). In addition, 18 transitions of Na (3p to 9-13d and 11-14s) and 10 of argon (5p-4s) were measured. Analysis of the spectrum indicates that perhaps all absorption signals are due to neutrals NaH, Na, and Ar and are observed via "population" modulation. Copyright 1997 Academic Press. Copyright 1997Academic Press

Journal Article↗
PubMed1997

Mechanisms of nitrate accumulation in plasma during pacing-induced heart failure in conscious dogs.

The goal of this study was to understand the mechanisms behind the changes in plasma NOx during heart failure. Heart failure is associated with an increase in plasma nitrate levels, and yet most experimental evidence demonstrates a reduction in endothelial nitric oxide production during heart failure. Dogs were chronically instrumented for measurement of systemic hemodynamics and left ventricular (LV) dimensions. Hearts were paced at 210 bpm for 3 weeks (n = 14) and then 240 bpm for 1 week (n = 7). Hemodynamics, arterial blood gases, plasma NOx, and creatinine levels were monitored weekly. Heart failure was evidenced by cachexia, ascites, and hemodynamic alterations. Resting heart rate rose (94 +/- 6 to 135 +/- 9 bpm), and LV dP/dt fell (2810 +/- 82 to 1471 +/- 99 mm Hg/s), while LV end diastolic pressure quadrupled (5.8 +/- 0.7 to 25 +/- 0.8 mm Hg), and diastolic wall stress quadrupled (11 +/- 1.3 to 43 +/- 6.0 g/cm2, all P < 0.05). These changes occurred during a doubling in plasma NOx (5.5 +/- 1.5 to 10 +/- 1.6 microM, P < 0.05). There were no changes in plasma NOx through 3 weeks of pacing. Plasma creatinine levels increased 450% (from 0.27 +/- 0.32 to 1.21 +/- 0.63 mg%). Stimulated nitrite production by agonists in sieved coronary microvessels was unchanged after 3 weeks of pacing but was reduced after heart failure. Plasma NOx did not correlate with LV dP/dt or systolic wall stress but correlated directly with LV EDP or diastolic wall stress and inversely with cardiac work. Plasma NOx rose in direct relation to plasma creatinine levels (Y = 4.8X + 2.8, r2 = 0.84), suggesting that the rise in plasma NOx during heart failure is due to decreased renal function not increased NO production.

Acetylcholine↗
PubMed1997

Association of angiotensin I-converting enzyme gene polymorphism with myocardial ischemia and patency of infarct-related artery in patients with acute myocardial infarction.

OBJECTIVES: We determined the influence of angiotensin I-converting enzyme (ACE) insertion (I)/deletion (D) polymorphism on the extent of myocardial ischemia in patients with acute myocardial infarction. BACKGROUND: The I/D polymorphism, which in part controls plasma and tissue expression of ACE, has been implicated in predisposition to myocardial infarction and ventricular remodeling. METHODS: I/D genotyping, predischarge adenosine-thallium-201 perfusion tomography and radionuclide angiography were performed in 113 patients (72 men, 41 women) with a diagnosis of acute myocardial infarction. A subgroup of 96 patients also underwent coronary angiography. RESULTS: Genotypes DD, ID and II were present in 27, 56 and 30 patients, respectively. There was no significant difference in the baseline characteristics of patients, total creatine kinase, peak MB fraction, Killip class, mean ejection fraction or the number of diseased vessels in patients with the DD, ID or II genotype. However, the size of the total and the reversible perfusion defects was greater in those with DD than in those with ID or II genotype (total defect size [mean +/- SD] 33.7 +/- 22.5%, 29.5 +/- 19.2% and 22.2 +/- 16.0%, respectively [p = 0.022]; reversible defect size 18.0 +/- 16.0%, 12.1 +/- 11.6% and 8.2 +/- 7.8%, respectively [p = 0.006]). Occlusion of the infarct-related artery was also more common in patients with DD genotype (odds ratio 3.9, 95% confidence interval 1.4 to 11.0). Multivariate analysis showed that the I/D genotype was an independent predictor of perfusion defect size and patency of the infarct-related artery (p = 0.001). CONCLUSIONS: DD genotype was associated with a larger ischemic defect and occlusion of the infarct-related artery. Patients with DD genotype, having a larger ischemic defect, are expected to be at a greater risk for subsequent cardiovascular events.

Adenosine↗
PubMed1997

A preliminary morphometric study on the endometrium from patients treated with indomethacin-releasing copper intrauterine device.

The intrauterine device (IUD) is an effective method of birth control. However, IUD-induced uterine bleeding is a major side-effect and always causes inconvenience, sometimes even anaemia. It has been reported that oral administration of indomethacin could can reduce IUD-induced uterine bleeding. In the present study, we investigated whether indomethacin-releasing copper IUD (IR-Cu-IUD) can prevent insertion-induced uterine bleeding and its mechanism. Nine healthy volunteers of reproductive age were selected for the study. Endometrial tissues were collected at same menstrual stage prior to and 3-6 months after IR-Cu-IUD insertion. Endometrial morphology, cell proliferation/differentiation, morphometry and activity of complement Factor VIII were examined. No significant difference was found in any of the parameters examined in the same patients, both prior to and after IR-Cu-IUD insertion. By comparison with data previously obtained from the patients who had Cu-IUD insertions, it is clear that IR-Cu-IUD markedly reduced IUD-induced uterine bleeding and this reduction is primarily contributed by the anti-inflammatory action of indomethacin.

Adult↗
PubMed1997

Identification, sequencing, and enzymatic activity of the erythrose-4-phosphate dehydrogenase gene of Vibrio cholerae.

We have identified a gene in Vibrio cholerae (epd) which encodes an erythrose-4-phosphate dehydrogenase activity and is located immediately downstream of an iron-regulated virulence gene, irgA, and immediately upstream of a gene encoding phosphoglycerate kinase (pgk). Expression of epd in V. cholerae is not regulated by iron, nor is it required for virulence in an infant mouse model.

Aldehyde Oxidoreductases↗
PubMed1997

Biochemical characterization of penicillin-resistant and -sensitive penicillin-binding protein 2x transpeptidase activities of Streptococcus pneumoniae and mechanistic implications in bacterial resistance to beta-lactam antibiotics.

To understand the biochemical basis of resistance of bacteria to beta-lactam antibiotics, we purified a penicillin-resistant penicillin-binding protein 2x (R-PBP2x) and a penicillin-sensitive PBP2x (S-PBP2x) enzyme of Streptococcus pneumoniae and characterized their transpeptidase activities, using a thioester analog of stem peptides as a substrate. A comparison of the k(cat)/Km values for the two purified enzymes (3,400 M(-1) s(-1) for S-PBP2x and 11.2 M(-1) s(-1) for R-PBP2x) suggests that they are significantly different kinetically. Implications of this finding are discussed. We also found that the two purified enzymes did not possess a detectable level of beta-lactam hydrolytic activity. Finally, we show that the expression levels of both PBP2x enzymes were similar during different growth phases.

Anti-Bacterial Agents↗
PubMed1997

Anoxia-reoxygenation versus ischemia in isolated rat lungs.

Oxidant generation in anoxia-reoxygenation and ischemia-reperfusion was compared in isolated rat lungs. Anoxia-reoxygenation was produced by N2 ventilation followed by O2 ventilation. After anoxia, lung ATP content was decreased by 59%. Oxygenated ischemia was produced by discontinuing perfusion while ventilation with O2 was maintained. With anoxia-reoxygenation, oxidant generation, evaluated by oxidation of dichlorodihydrofluorescein (H2DCF) to fluorescent dichlorofluorescein, increased 3.6-fold, lung thiobarbituric acid reactive substances (TBARS) increased 342%, conjugated dienes increased 285%, and protein carbonyl content increased 46%. Pretreatment of lungs with 100 microM allopurinol inhibited the reoxygenation-mediated increase in lung fluorescence by 75% and TBARS by 69%. Oxygenated ischemia resulted in an approximately eightfold increase in lung H2DCF oxidation and a fourfold increase in TBARS, but allopurinol had no effect. On the other hand, 100 microM diphenyliodonium (DPI) inhibited the ischemia-mediated increase in lung fluorescence by 69% and lung TBARS by 70%, but it had no effect on the increase with anoxia-reoxygenation. Therefore, both ischemia-reperfusion and anoxia-reoxygenation result in oxidant generation by the lung, but a comparison of results with a xanthine oxidase inhibitor (allopurinol) and a flavoprotein inhibitor (DPI) indicate that the pathways for oxidant generation are distinctly different.

Adenosine Triphosphate↗
PubMed1997

Short-term exercise training enhances reflex cholinergic nitric oxide-dependent coronary vasodilation in conscious dogs.

The effects of exercise training on the coronary vasodilation following activation of the Bezold-Jarisch reflex were examined in conscious dogs. Mongrel dogs were chronically instrumented using sterile techniques for measurements of systemic hemodynamics and left circumflex coronary blood flow (CBF). With the heart rate controlled (150 bpm), veratrine (0.5 to 20 micrograms/kg) caused dose-dependent increases in CBF; eg, 5 micrograms/kg of veratrine increased CBF by 61 +/- 6% from 31 +/- 1.3 mL/min (P < .05). After exercise training, the dose-response curve of CBF in response to veratrine was shifted to the left; eg, 5 micrograms/kg of veratrine increased CBF by 101 +/- 12% (P < .05 compared with control) from 34 +/- 2.3 mL/min. The enhanced coronary vasodilation was blunted by nitro-L-arginine (NLA, 35 mg/kg). In anesthetized dogs after exercise training, electrical stimulation of the left vagus nerve caused greater increases in CBF, and NLA inhibited increases in CBF. Acetylcholine, norepinephrine, angiotensin II, and bradykinin caused greater increases in NO2- production in coronary microvessels from exercise-trained dogs compared with those from normal dogs. Our results indicate that the coronary vasodilation following activation of the Bezold-Jarisch reflex is enhanced in conscious dogs after exercise training. Since electrical stimulation of the vagus nerve caused greater coronary vasodilation and since the agonists resulted in greater increases in NO production in coronary microvessels from exercise-trained dogs, the mechanism responsible for the enhanced coronary vasodilation following activation of the Bezold-Jarisch reflex is most likely due to the increased release of NO from the endothelial cells.

Acetylcholine↗
PubMed1997

Expression of a mutant (Arg92Gln) human cardiac troponin T, known to cause hypertrophic cardiomyopathy, impairs adult cardiac myocyte contractility.

The mechanism(s) by which mutations in sarcomeric proteins cause hypertrophic cardiomyopathy (HCM) remains unknown. A leading hypothesis proposes that mutant sarcomeric proteins impair cardiac myocyte contractility, providing an impetus for compensatory hypertrophy. To test this hypothesis, we determined the impact of expression of a mutant (Arg92Gln) human cardiac troponin T (cTnT), known to cause HCM in humans, on adult cardiac myocyte contractility. A full-length human cTnT cDNA was cloned, and the Arg92Gln mutation was induced. Recombinant adenoviruses Ad5/CMV/cTnT-N and Ad5/CMV/cTnT-Arg92Gln were generated through homologous recombination. Adult feline cardiac myocytes were infected with recombinant adenoviruses or a control viral vector (Ad5 delta E1) at a multiplicity of infection of 100. Expression levels of the full-length normal and mutant cTnT proteins were equal on Western blots. Expression of the exogenous cTnT proteins in cardiac myocytes was also shown by immunocytochemistry and immunofluorescence, and their incorporation into myofibrils was confirmed by Western blotting on myofibrillar extracts. Electron microscopy showed intact sarcomere structure in rod-shaped cardiac myocytes in all groups. Cell fractional shortening and the peak velocity of shortening were not significantly different among the groups 24 hours after transduction. However, 48 hours after transduction, both fractional shortening and the peak velocity of shortening were significantly reduced (24% [P < .001] and 26% [P < .001], respectively) in cardiac myocytes in the Ad5/CMV/cTnT-Arg92Gln compared with the Ad5/CMV/cTnT-N groups. The magnitude of the reductions was greater at 72 hours after transduction (45% and 39%, respectively; P < .001). Our results indicated that expression of the mutant (Arg92Gln) cTnT, known to cause HCM in humans, impaired intact adult cardiac myocyte contractility. Our data also show that both normal and mutant cTnT were incorporated into myofibrils. These results provide a potential mechanism by which mutations in sarcomeric proteins cause HCM.

Adult↗
PubMed1997

Role of iron in ischemia-reperfusion oxidative injury of rat lungs.

We have previously shown that isolated, oxygen-ventilated rat lungs generate reactive oxygen species during ischemia and reperfusion. To evaluate the role of free iron in lung ischemia/reperfusion injury, we measured desferrioxamine-chelatable iron (DC-Fe), protein carbonyls, and thiobarbituric acid reactive substances (TBARS) in lungs subjected to global ischemia and reperfusion. There were no changes in DC-Fe, TBARS, or protein carbonyls during 2 h of control perfusion. There was a 2.3-fold increase in DC-Fe during 1 h ischemia and a further doubling during reperfusion. Results were similar when lungs were ventilated with O2 or N2. Lung TBARS increased 214% during ischemia/reperfusion with oxygen ventilation; unlike DC-Fe release, this change was blocked by N2 ventilation. Protein carbonyl content of the lung also increased significantly (113%) with ischemia/reperfusion. Ferric 8-hydroxyquinoline added to the perfusate before ischemia increased DC-Fe in lung tissue and significantly enhanced the lipid and protein oxidation of ischemic/reperfused lungs. The added perfusate iron had no effect on control lungs. Proteins isolated from the iron-supplemented ischemic/reperfused lungs were resistant to further in vitro oxidation induced by hydrogen peroxide (30 microM) whereas proteins from control perfused lungs were oxidized under these conditions. These results indicate that DC-Fe plays an important role in lung oxidative injury with ischemia/reperfusion. DC-Fe is released from iron-storage sites during ischemia and promotes tissue oxidation when oxygenation is maintained during ischemia or restored during reperfusion.

Animals↗
PubMed1997

[Research on types of Salmonella in some animals in Jilin province].

Some animals were examined for the presence of Salmonella in Jilin province. The rate of Salmonella detection was 537 strains from 846 snakes samples (63.5%); 136 strains from 648 frog samples (20%); 185 strains from 369 pig and chick samples (50%). All isolated Salmonella comprised of two subgenus (SII and SIIIb). Serologically, groups 04, 07, 08, 09, 01, 03, 19, 03, 10, 016, 035, 043, 048, 050, 058 and 061 were identified and the isolates were classified into 13 groups and 24 serotypes. Two of these isolates SII43:enZ15:1, 6 and SIIIb58:Z52:Z are reported for the first time in China.

Animals↗
PubMed1997

[Inherited defect of platelet nitric oxide synthase activity in essential hypertension].

The collagen-provocated platelet nitric oxide synthase (NOS) activity by the method of 3H-labelled L-arginine was compared between 19 essential hypertensives (EH) and 21 controls, and between 13 adolescents with their both parent hypertensives (FH+) and 12 adolescents without genetic hypertensive predisposition (FH-) as well. Results showed that the platelet NOS activity was lower significantly in EH group (4.76 +/- 2.01 vs 8.09 +/- 2.36 pmol.g-1.min-1, P < 0.001) and in FH+ group (3.64 +/- 2.07 vs 5.51 +/- 2.13 pmol.g-1.min-1, P < 0.05) comparing with their control groups respectively. It suggests that the inherited defect of some anti-hypertensive mechanisms like NO/NOS system may be implicated in the development of EH, which can be taken as a new "genetic marker" for detecting of specific clinic subtype. An useful data was thus presented of value in screening referred genes, for early prevention and rational remedy in essential hypertension.

Adolescent↗
PubMed1997

Application of fuzzy graph theory to evaluation of human cardiac function.

To explore the possibility of application of the fuzzy graph theory to the evaluation of human cardiac function, the cardiac function of two groups of personnel working under special environment were evaluated using the method of fuzzy graph theory. The first group consists of 31 subjects aged 19-21 years. They were classified according to their cardiac function evaluated by the method of maximum support tree. While the second group consists of 24 subjects aged 30-40 years and were classified with fuzzy graph theory on the basis of 6 maximum principal components extracted from 16 physiological indices. Medical explanation of the results is convincing.

Adult↗
PubMed1997

[Antianoxic effects of Dracocephalum tanguticum on brain of mice].

The aqueous extracts i.p. of Dracocephalum tanguticum Maxim (DtM), a Tibetan medicine, prolong sighificantly decapitaion-induced gasping duration in mice and the survival time of mice ligated bilateral carotid (P > 0.01). DtM prolong also the primal gasping in mice after injecting the air into the coccygeal vein (P > 0.01) and the survival time in mice poisoned by Lidocaine (P > 0.05). In addition, DtM is possessed of protecting against the pathologic lession of brain in rats under stimulating high altitude hypoxic condition. The results suggest that DtM has a antianoxic effects on mice.

Animals↗
PubMed1997

[Detection of hepatitis G virus RNA in sera in non A-E hepatitis patients using polymerase chain reaction with multiple set primers].

A double polymerase chain reaction, involoving nested primers deduced from NS3-5 regions of the hepatitis G virus (GBV-c/HGV) genome, was developed for a sensitive and specific detection of GBV-C (HGV) RNA. With this method, 10 anti-HGV positive patients with non A-E hepatitis and 10 healthy subjects were tested. Among 10 patients, GBV-C RNA was detected in 9, 8, 4, 9 patients by the NS-3 (1) primers, the NS3(2) primers, the NS4 primers, the NS5(1) primers and the NS5(2) primers respectively. Control sera from 10 healthy subjects did not reveal GBV-C (HGV) RNA by any set of the primers. These data suggest that the detection rate of GBV-C (HGV) RNA is different in various set of primers, the NS3(1) and the NS5(2) primers are superior to other primers and are more suitable for RT-PCR of GBV-C (HGV) RNA.

DNA Primers↗
PubMed1997

[Separation of soybean agglutinin by hydrophobic-interaction chromatography].

The soybean agglutinin (SBA) was separated with hydrophobic-interaction chromatography (HIC) in this work. HIC of the crude lectin extract of SBA was performed on Phenyl-Sepharose CL-4B column, 10 cm x 2.5 cm i.d., at a flow-rate of 1.0 mL/min. A 20 mL sample of the crude extract was applied to the column previously equilibrated with the buffer, 0.01 mol/L PBS containing ammonium sulfate (60% of saturation concentration). The column was eluted with the starting buffer, then with the buffer containing 30% saturation of ammonium sulfate, and finally with 0.01 mol/L PBS. Fractions were detected by UV absorbance at 280 nm and assayed for hemagglutinating activity. The results show that the purification-fold was as high as 35 and the recovery of activity was 100%.

Chromatography↗